The plant defense hormone salicylic acid (SA) is perceived by two classes of receptors, NPR1 and NPR3/NPR4. They function in two parallel pathways to regulate SA-induced defense gene expression. To better understand the roles of the SA receptors in plant defense, we systematically analyzed their contributions to different aspects of Arabidopsis (Arabidopsis thaliana) plant immunity using the SA-insensitive npr1-1 npr4-4D double mutant. We found that perception of SA by NPR1 and NPR4 is required for activation of N-hydroxypipecolic acid biosynthesis, which is essential for inducing systemic acquired resistance. In addition, both pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) are severely compromised in the npr1-1 npr4-4D double mutant. Interestingly, the PTI and ETI attenuation in npr1-1 npr4-4D is more dramatic compared with the SA-induction deficient2-1 (sid2-1) mutant, suggesting that the perception of residual levels of SA in sid2-1 also contributes to immunity. Furthermore, NPR1 and NPR4 are involved in positive feedback amplification of SA biosynthesis and regulation of SA homeostasis through modifications including 5-hydroxylation and glycosylation. Thus, the SA receptors NPR1 and NPR4 play broad roles in plant immunity.

植物防御激素水杨酸 (SA) 被两类受体 NPR1 和 NPR3/NPR4 感知。它们通过两条平行途径发挥作用，调节 SA 诱导的防御基因表达。为了更好地了解SA受体在植物防御中的作用，我们使用SA不敏感的npr1-1 npr4-4D双突变体系统分析了它们对拟南芥（ Arabidopsis thaliana ）植物免疫的不同方面的贡献。我们发现 NPR1 和 NPR4 对 SA 的感知是N-羟基哌啶酸生物合成激活所必需的，这对于诱导系统获得性耐药至关重要。此外，模式触发免疫（PTI）和效应触发免疫（ETI）在npr1-1 npr4-4D双突变体中均受到严重损害。有趣的是，与SA 诱导缺陷 2-1 ( sid2-1 ) 突变体相比， npr1-1 npr4-4D中的 PTI 和 ETI 衰减更为显着，这表明sid2-1中 SA 残留水平的感知也有助于免疫。此外，NPR1 和 NPR4 通过 5-羟基化和糖基化等修饰参与 SA 生物合成的正反馈放大和 SA 稳态的调节。因此，SA受体NPR1和NPR4在植物免疫中发挥着广泛的作用。